WGU C785 Final Exam Actual Exam 2026/2027 –
Comprehensive Biochemistry Assessment with Detailed
Rationales | 100% Verified | Pass Guaranteed – A+ Graded
SECTION A: CELLULAR METABOLISM & BIOENERGETICS -
GLYCOLYSIS, TCA, & OXIDATIVE PHOSPHORYLATION (Questions 1-10)
Q1: A 24-year-old male presents to the emergency department after a marathon with
severe muscle cramps and dark urine. Laboratory studies reveal elevated serum
creatine kinase and myoglobinuria. His muscle biopsy shows normal glycogen stores
but impaired ATP production during ischemic exercise. Which enzyme deficiency MOST
likely explains his inability to generate ATP from glycogen under anaerobic conditions?
A. Glucose-6-phosphatase
B. Pyruvate kinase [CORRECT]
C. Phosphofructokinase-1
D. Glycogen phosphorylase
Correct Answer: B
Rationale: Pyruvate kinase catalyzes the final step of glycolysis, converting
phosphoenolpyruvate (PEP) to pyruvate and generating ATP. A deficiency prevents ATP
production in the absence of oxygen, as pyruvate cannot enter aerobic metabolism.
Glucose-6-phosphatase deficiency (von Gierke disease) causes hypoglycemia and lactic
acidosis but not exercise-induced myoglobinuria. PFK-1 deficiency (Tarui disease)
causes similar symptoms but with glycogen accumulation. Glycogen phosphorylase
,deficiency (McArdle disease) presents with exercise intolerance but normal lactate
response to ischemic exercise.
Q2: A patient with type 2 diabetes is prescribed metformin, which inhibits complex I of
the electron transport chain. During oxidative phosphorylation, which complex is the
ONLY site where protons are pumped from the mitochondrial matrix to the
intermembrane space using energy derived directly from NADH oxidation?
A. Complex II (succinate dehydrogenase)
B. Complex III (cytochrome bc1 complex)
C. Complex I (NADH dehydrogenase) [CORRECT]
D. Complex IV (cytochrome c oxidase)
Correct Answer: C
Rationale: Complex I (NADH dehydrogenase) is the only complex that directly oxidizes
NADH, transferring electrons to ubiquinone while simultaneously pumping 4 protons
across the inner mitochondrial membrane. Complex II does not pump protons; it
accepts electrons from FADH2. Complex III pumps protons but uses energy from
ubiquinol oxidation, not directly from NADH. Complex IV pumps protons using energy
from cytochrome c oxidation.
Q3: A nurse is reviewing the biochemistry of the TCA cycle with a patient newly
diagnosed with mitochondrial myopathy. The patient asks which intermediate is BOTH a
product of the TCA cycle and a substrate for gluconeogenesis. Which intermediate
serves this dual role?
A. Acetyl-CoA
,B. Oxaloacetate [CORRECT]
C. Citrate
D. α-Ketoglutarate
Correct Answer: B
Rationale: Oxaloacetate is the final product of the TCA cycle (regenerated from malate)
and is also the starting substrate for gluconeogenesis, where it is converted to
phosphoenolpyruvate via PEP carboxykinase. Acetyl-CoA cannot be used for net
glucose synthesis in humans because the pyruvate dehydrogenase reaction is
irreversible. Citrate and α-ketoglutarate are TCA intermediates but are not direct
gluconeogenic substrates.
Q4: During a fasting state, a patient's hepatocytes are performing gluconeogenesis.
Which allosteric regulator simultaneously activates gluconeogenesis while inhibiting
glycolysis, ensuring these opposing pathways do not operate simultaneously?
A. Fructose-2,6-bisphosphate
B. Citrate
C. Acetyl-CoA [CORRECT]
D. AMP
Correct Answer: C
Rationale: Acetyl-CoA allosterically activates pyruvate carboxylase (the first committed
step of gluconeogenesis) while simultaneously inhibiting pyruvate dehydrogenase
(which converts pyruvate to acetyl-CoA, committing it to the TCA cycle). This ensures
, pyruvate is diverted toward glucose synthesis rather than oxidation.
Fructose-2,6-bisphosphate activates glycolysis and inhibits gluconeogenesis. Citrate
inhibits phosphofructokinase-1 (glycolysis) but does not directly activate
gluconeogenesis. AMP activates glycolysis and inhibits gluconeogenesis.
Q5: A patient presents with lactic acidosis after receiving a large dose of intravenous
fructose. Fructose metabolism bypasses which rate-limiting enzyme of glycolysis,
allowing rapid unregulated ATP depletion and lactic acid production?
A. Hexokinase
B. Phosphofructokinase-1 [CORRECT]
C. Pyruvate kinase
D. Glyceraldehyde-3-phosphate dehydrogenase
Correct Answer: B
Rationale: Fructose is phosphorylated to fructose-1-phosphate by fructokinase, then
cleaved by aldolase B to dihydroxyacetone phosphate (DHAP) and glyceraldehyde.
DHAP enters glycolysis downstream of phosphofructokinase-1 (PFK-1), the primary
rate-limiting enzyme of glycolysis. This bypass allows rapid, unregulated flux through
glycolysis, depleting ATP (fructokinase consumes ATP) and overwhelming the pyruvate
dehydrogenase complex, shunting pyruvate to lactate. Hexokinase is bypassed by
fructokinase but is not the primary rate-limiting step.
Q6: A 45-year-old male with chronic alcoholism presents with Wernicke-Korsakoff
syndrome. His thiamine (vitamin B1) deficiency impairs which enzyme complex that is
essential for both the TCA cycle and the conversion of pyruvate to acetyl-CoA?
Comprehensive Biochemistry Assessment with Detailed
Rationales | 100% Verified | Pass Guaranteed – A+ Graded
SECTION A: CELLULAR METABOLISM & BIOENERGETICS -
GLYCOLYSIS, TCA, & OXIDATIVE PHOSPHORYLATION (Questions 1-10)
Q1: A 24-year-old male presents to the emergency department after a marathon with
severe muscle cramps and dark urine. Laboratory studies reveal elevated serum
creatine kinase and myoglobinuria. His muscle biopsy shows normal glycogen stores
but impaired ATP production during ischemic exercise. Which enzyme deficiency MOST
likely explains his inability to generate ATP from glycogen under anaerobic conditions?
A. Glucose-6-phosphatase
B. Pyruvate kinase [CORRECT]
C. Phosphofructokinase-1
D. Glycogen phosphorylase
Correct Answer: B
Rationale: Pyruvate kinase catalyzes the final step of glycolysis, converting
phosphoenolpyruvate (PEP) to pyruvate and generating ATP. A deficiency prevents ATP
production in the absence of oxygen, as pyruvate cannot enter aerobic metabolism.
Glucose-6-phosphatase deficiency (von Gierke disease) causes hypoglycemia and lactic
acidosis but not exercise-induced myoglobinuria. PFK-1 deficiency (Tarui disease)
causes similar symptoms but with glycogen accumulation. Glycogen phosphorylase
,deficiency (McArdle disease) presents with exercise intolerance but normal lactate
response to ischemic exercise.
Q2: A patient with type 2 diabetes is prescribed metformin, which inhibits complex I of
the electron transport chain. During oxidative phosphorylation, which complex is the
ONLY site where protons are pumped from the mitochondrial matrix to the
intermembrane space using energy derived directly from NADH oxidation?
A. Complex II (succinate dehydrogenase)
B. Complex III (cytochrome bc1 complex)
C. Complex I (NADH dehydrogenase) [CORRECT]
D. Complex IV (cytochrome c oxidase)
Correct Answer: C
Rationale: Complex I (NADH dehydrogenase) is the only complex that directly oxidizes
NADH, transferring electrons to ubiquinone while simultaneously pumping 4 protons
across the inner mitochondrial membrane. Complex II does not pump protons; it
accepts electrons from FADH2. Complex III pumps protons but uses energy from
ubiquinol oxidation, not directly from NADH. Complex IV pumps protons using energy
from cytochrome c oxidation.
Q3: A nurse is reviewing the biochemistry of the TCA cycle with a patient newly
diagnosed with mitochondrial myopathy. The patient asks which intermediate is BOTH a
product of the TCA cycle and a substrate for gluconeogenesis. Which intermediate
serves this dual role?
A. Acetyl-CoA
,B. Oxaloacetate [CORRECT]
C. Citrate
D. α-Ketoglutarate
Correct Answer: B
Rationale: Oxaloacetate is the final product of the TCA cycle (regenerated from malate)
and is also the starting substrate for gluconeogenesis, where it is converted to
phosphoenolpyruvate via PEP carboxykinase. Acetyl-CoA cannot be used for net
glucose synthesis in humans because the pyruvate dehydrogenase reaction is
irreversible. Citrate and α-ketoglutarate are TCA intermediates but are not direct
gluconeogenic substrates.
Q4: During a fasting state, a patient's hepatocytes are performing gluconeogenesis.
Which allosteric regulator simultaneously activates gluconeogenesis while inhibiting
glycolysis, ensuring these opposing pathways do not operate simultaneously?
A. Fructose-2,6-bisphosphate
B. Citrate
C. Acetyl-CoA [CORRECT]
D. AMP
Correct Answer: C
Rationale: Acetyl-CoA allosterically activates pyruvate carboxylase (the first committed
step of gluconeogenesis) while simultaneously inhibiting pyruvate dehydrogenase
(which converts pyruvate to acetyl-CoA, committing it to the TCA cycle). This ensures
, pyruvate is diverted toward glucose synthesis rather than oxidation.
Fructose-2,6-bisphosphate activates glycolysis and inhibits gluconeogenesis. Citrate
inhibits phosphofructokinase-1 (glycolysis) but does not directly activate
gluconeogenesis. AMP activates glycolysis and inhibits gluconeogenesis.
Q5: A patient presents with lactic acidosis after receiving a large dose of intravenous
fructose. Fructose metabolism bypasses which rate-limiting enzyme of glycolysis,
allowing rapid unregulated ATP depletion and lactic acid production?
A. Hexokinase
B. Phosphofructokinase-1 [CORRECT]
C. Pyruvate kinase
D. Glyceraldehyde-3-phosphate dehydrogenase
Correct Answer: B
Rationale: Fructose is phosphorylated to fructose-1-phosphate by fructokinase, then
cleaved by aldolase B to dihydroxyacetone phosphate (DHAP) and glyceraldehyde.
DHAP enters glycolysis downstream of phosphofructokinase-1 (PFK-1), the primary
rate-limiting enzyme of glycolysis. This bypass allows rapid, unregulated flux through
glycolysis, depleting ATP (fructokinase consumes ATP) and overwhelming the pyruvate
dehydrogenase complex, shunting pyruvate to lactate. Hexokinase is bypassed by
fructokinase but is not the primary rate-limiting step.
Q6: A 45-year-old male with chronic alcoholism presents with Wernicke-Korsakoff
syndrome. His thiamine (vitamin B1) deficiency impairs which enzyme complex that is
essential for both the TCA cycle and the conversion of pyruvate to acetyl-CoA?
